The biochemical communication pathways initiated by hormones that suppress appetite and promote satiety, thereby contributing to the regulation of energy balance. Key hormones involved in this signaling include leptin, cholecystokinin (CCK), and peptide YY (PYY), which act on specific receptors in the hypothalamus and brainstem. Effective signaling in this system is vital for maintaining a healthy body weight and preventing metabolic dysfunction.
Origin
The term is derived from the Greek roots an- (without) and orexis (appetite), combined with hormone (to set in motion) and signaling (the transmission of a message). This framework describes the system responsible for generating the physiological message of “fullness.” It originates conceptually within the broader study of neuroendocrinology and energy homeostasis.
Mechanism
Following food intake, various gut and adipose-derived hormones are released into the circulation, traveling to the central nervous system. These anorexigenic signals bind to their respective receptors, particularly on neurons in the arcuate nucleus of the hypothalamus, such as the POMC neurons. This receptor activation leads to downstream neuronal firing and neurotransmitter release, ultimately translating the hormonal message into the behavioral outcome of reduced food intake and increased energy expenditure.
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